A small fraction of mammalian genes exhibit parent-of-origin specific monoallelic expression. They are expressed from only one allele and this is determined by modifications established in the germline. Approximately 100 imprinted genes have been identified to date. Most imprinted genes are located in discrete clusters and are controlled by shared regulatory elements. Imprinted genes play important roles in regulating embryonic and placental development, with overt growth phenotypes resulting both from loss of expression and from over-expression of imprinted genes. The maternally expressed Phlda2 gene has been implicated in placental development. Loss of expression leads to placentomegaly as a consequence of the disproportionate expansion of the spongiotrophoblast layer. In this study, the consequences of over-expressing Phlda2 and the adjacent Slc22a18 were investigated in four independent lines of transgenic mice driving incrementally increasing doses of the two genes and on two genetic backgrounds. In all cases, transgenic placentae were significantly lighter throughout gestation, which was entirely due to a reduction in the spongiotrophoblast layer. There was also a reduction in glycogen staining and a progressive mislocalisation of cells from the spongiotrophoblast layer. These phenotypes were essentially restored by restored by normalising Phlda2 gene dosage in a single copy line. In addition, transgenic embryos were significantly lighter than wild type littermates from E16.5 onwards and were born 13% lighter. These embryos were asymmetrically growth restricted and displayed rapid post-natal catch up growth within two weeks of birth. Adult transgenic females that had undergone embryonic growth restriction also displayed increased adiposity and reduced glucose tolerance at one year of age. These data suggest that altered expression of Phlda2 and possibly Slc22a18 drive IUGR and program adult disease susceptibility. Recent human studies have found an association between elevated placental PHLDA2 and low birth weight or IUGR infants. This mouse model may thus provide a genetic tool that recapitulates a known human condition for further investigation of the fetal programming of metabolic syndrome.